Neonatal rats were given aqueous lead acetate intragastrically from d 2-20 of life at doses of 0, 25, 75, and 225 mg Pb/kg·d. Blood Pb concentrations on d 21 were (mean ± SE) 27 ± 4 (control), 150 ± 26, 263 ± 63, and 518 ± 97 μg/100 ml, respectively. Growth was significantly depressed only in animals given the highest dose of Pb (225 mg/kg·d). Hematocrits were significantly decreased by d21 at all doses of Pb. Malondialdehyde (MDA) formation in 750 X g (10 min) brain supernatants induced spontaneously by aerobic incubation at 37°C was not altered by Pb on d 7 and 14, but a slight decrease was observed on d 21. The extent of MDA formation induced by enzymatically generated superoxide anion was not altered by Pb toxicity during the first 21 d of life. Addition of Pb to 750 X g (10 min) brain supernatants in vitro significantly decreased MDA formation at Pb concentrations of 10-5 M and higher. These results show that the central nervous system toxicity of Pb in neonatal rats is not associated with accelerated in vitro Iipid peroxidation of brain tissue.
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